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Intrauterine Growth RestrictionIntrauterine Growth Restriction
(IUGR)(IUGR)
Dr. Amlendra Kumar YadavDr. Amlendra Kumar Yadav
Definition
Failure of the fetus to reach growth potential
associated with increased morbidity and
mortality
Ponderal index less than 10th
centile.
(used to identify infants whose soft tissue mass is bellow normal for the stsge of
skeletal development)
Birthweight x 100
Ponderal index = Crown –heel length³
IUGR Facts
• IUGR associated with 3-10 % of all
pregnancies
• Perinatal mortality rate is 5-20 times higher for
growth retarded fetuses .
• 2nd
leading contributor to the Perinatal mortality
rate
• 20% of all stillbirths are IUGR
• Incidence of intrapartum asphyxia in cases of
IUGR has been reported to be 50%.
• Early and proper identification and management
lowers this perinatal mortality and morbidity
Incidence of IUGR in Bangladesh
According to National Low Birth Weight Survey
of Bangladesh
Low birth weight (<2500g) affects 36% of infants
in Bangladesh
At least 77% of LBW infants were growth
retarded
Normal Fetal Growth
• Normal fetal growth is characterized by
cellular hyperplasia followed by
hyperplasia and hypertrophy and lastly by
hypertrophy alone.
Normal Intrauterine Growth
Stage 1 Stage 2 Stage 3
Hyperplasia Hyperplasia/ hypertrophy Hypertrophy
4-20 weeks 20-28 weeks 28-40 weeks
Rapid mitosis Declining mitosis Rapid hypertrophy
Increasing DNA content Increasing cell size Rapid increasing cell size
rapid accumulation of fat,
muscle, connective tissue
Symmetric Mixed- asymmetric Asymmetric
Weight gain
• Fetal growth accelerates from about 5g per
day at 14 -15 wks of gestation to
• 10g per day at 20 wks
• Peaks at 30 -35g per day at 32-34wks
• After which growth rate decreases.
Fetal Growth Indices
• Symphysiofundal height increases by about
1cm per wk between 14 and 32 wks.
• Abdominal girth increases by 1 inch per wk
after 30 wks. It is about 30 inches at 30wks in
an average built woman.
Classification of Inrauterine Growth Restriction
1. Symmetrical IUGR
2. Asymmetrical IUGR
Symmetrical IUGR
Head circumference, length, and weight are all proportionally
reduced for grstational age (below 10th
percentile).
It is due to either decreased growth potential of the fetus or
extrinsic conditions that are active in pregnancy .
Asymmetrical IUGR
Fetal weight is reduced out of proportion to length and head
circumference .
The usual causes are uteroplacental insufficiency, maternal
malnutrition, or extrinsic conditions appearing late in pregnancy.
Aetiology
• IUGR is a manifestation of fetal, maternal and
placental disorders that affect fetal growth.
A.Fetal Causes
1. Chromosomal Disorders-
usually result in early onset IUGR.
 Trisomies 13, 18, 21 contribute to 5% of IUGR cases
 Sex chromosome disorders are frequently lethal,
fetuses that survive may have growth restriction
(Turner Syndrome)
Fetal causes contd..
2. Congenital Infections:
• The growth potential of fetus may be severely
impaired by intrauterine infections.
• The timing of infection is crucial as the resultant
effects depends on the phase of organogenesis.
• Viruses- rubella, CMV, varicella and HIV
 rubella is the most embryotoxic virus, it cause capillary
endothelial damage during organogenesis and impairs fetal
growth.
 CMV causes cytolysis and localized necrosis in fetus.
• Protozoa- like malaria, toxoplasma, trypanosoma
have also been associated with growth restriction.
Fetal causes contd..
3. Structural Anomalies-
All major structural defects involving
CNS,CVS,GIT, Genitourinary and musculoskeletal
system are associated with increased risk of fetal
growth restriction.
If growth restriction is associated with
polyhydramnios, the incidence of structural
anomaly is substantially increased.
Fetal causes contd..
4. Genetic Causes-
Maternal genes have greater influence on
fetal growth.
Inborn errors of metabolism like agenesis
of pancreas, congenital lipodystrophy,
galactosemia, phenylketonuria also result in
growth restriction of fetus.
B. Placental causes
• Placenta is the sole channel for nutrition and
oxygen supply to the fetus.
Single umblical artery
abnormal placental implantation
velamentous umblical cord insertion
bilobed placenta
placental haemangiomas have all been associated
with fetal growth restriction
C. Maternal Causes
1. Maternal Characteristics:
those contributing to IUGR are-
 Extremes of maternal age
 Grandmultiparity
 History of IUGR in previous pregnancy
 Low maternal weight gain in pregnancy
2. Maternal diseases:
Uteroplacental insufficiency resulting from
medical complications like
 Hypertension
 Renal disease
 Autoimmune disease
 Hyperthyroidism
 Long term insulin dependent diabetes
Maternal causes contd..
• Smoking- active or passive, especially during
third trimester is important cause of IUGR.
Nicotine has vasoconstrctive effect on the
maternal circulation and leads to formaton of
toxic metabolites in fetus.
• Alchohol and Drugs- Alchohol crosses the
placenta freely. It acts as a cellular poison
reducing fetal growth potential.
• Cocaine and opiates are potent vasoconstrictors.
• Warfarin, anticonvulsants and antineoplastic
agents are also implicated in growth restriction
• Thrombophilias- antiphospholipid antibody
syndrome and other thrombophilias leading to
placental thrombosis and impaired trophoblastic
function.
• Nutritional Deficiency- leads to deficient substrate
supply to the fetus
Diagnosis of IUGR
Identifying mothers at risk:
Poor maternal nutrition
Poor BMI at conception
Pre-eclampsia
Renal disorders
Diseases causes vascular insufficiency
Infections (TORCH)
Poor maternal wt. gain during pregnancy
• Determination of gestational age is of utmost
importance-
– Can be calculated from the date of LMP- not
reliable
– Ultrasound dating before 21 wks of pregnancy
provides more accurate estimate.
Diagnosis of IUGR
1. Clinically- Serial measurement of fundal
height and abdominal girth.
 Symphysio-fundal height normally increases by
1cm per wk b/w 14 and 32 wks.
 A lag in fundal ht. of 4wks is suggestive of
moderate IUGR.
 A lag of >6 wks is suggestive of severe IUGR.
Sonographic evaluation-
Fetal biometry:
i. BPD(Biparietal Diameter)- When growth rate of
BPD is below 5th
percentile, 82% of births are
below 10th
percentile
ii. Abdominal circumference AC and fetal wt are
most accurate ultrasound parameters for
diagnosis of IUGR.
AC < 5mm/wk reduction is suggestive of IUGR
iii. Measurement ratios- there are some age
independent ratios to detect IUGR
HC/AC: Persistence of a head to abdomen ratio <1
late in gestation is predictive of asymmetric IUGR.
Femur length : serial measurements of femur length
are effective for detecting symmetric IUGR
 Placental Morphology: Acceleration of
placental maturation may occur with IUGR .
 Placental volume: helpful in predicting
subsequent fetal growth.
 Amniotic fluid volume:
Amniotic fluid index(AFI) between 8 and 25 is
normal.
Doppler Ultrasonography
Doppler flow studies are important adjuncts to
fetal biometry in identifying the IUGR fetuses at
risk of adverse outcome.
Uterine artery flow abnormalities: predict IUGR
as early as 12-14 wks of gestation
Umblical Artery doppler:- In IUGR there is increased
umblical artery resistance
Middle cerebral artery doppler: in a normal
fetus has relatively little flow during diastole.
Increased resistance to blood flow in placenta
results in redistribution of cardiac output to
favour cardiac and cerebral circulations
leading to increased flow in the diastolic
phase
Ductus venosus doppler
In the normal fetus, flow in the ductus venosus is
forwards , moving towards the heart during entire
cardiac cycle.
When circulatory compensation of the fetus fails,
the ductus venosus waveform shows absent or
reverse blood flow during atrial contraction.
Perinatal mortality being 63-100%.
Sequential changes of doppler studies in decompensating fetal
growth restriction
Initial changes Decreased amniotic fluid index
Increased uterine artery resistance with EDV
Early changes
(in 50% 2-3 wks before nonreactive FHR)
Decreased MCA resistance (brain sparing )
Absent uterine artery EDV
Late changes
~ 6 days before nonreactive FHR
Increased resistance in DV-reversed EDV in
uterine artery
Very late changes
(in 70%, 24 hrs before changes in BPP)
Reversed flow in DV and pulsatile flow in
umbilical vein
( BPP- biophysical profile , DV- ductus venosus, EDV – end diastolic
velocity, FHR- fetal heart rate , MCA – mmiddle cerebral artery )
Placental magnetic resonance
imaging :
• Asses severity of fetal growth retardation on
the basis of decreased placental volume and
thickness.
Neonatal Assessment
• Reduced birth weight for gestational age
• Physical appearance: thin loose, peeling skin,
scaphoid abdomen, dispropotionately large
head
• Appropriate growth charts should be used
• Ponderal index
• Ballard score
MANAGEMENT
 Principles:
1. Identify the cause of growth restriction.
2. Treat the cause if found.
3. General management
MANAGEMENT
 First step is to identify the aetiology of IUGR:-
Maternal history pertaining to the risk factors of
IUGR.
Clinical examination- maternal habitus, height,
weight, BP etc.
Laboratory investigations
Hb, HCT to detect polycythemia
Blood sugar
Renal function tests,
Serology for TORCH
Fetal evaluation
• Ultrasound for growth restriction, amniotic
fluid, congenital anomalies and
• Doppler evaluation
Treatment of underlying cause
 Hypertension,
 Cessation of smoking,
 Protein energy supplementation in poorly
nourished and underweight women.
General Management
 Bed rest in left lateral position to increase
uteroplacental blood flow
 Maternal nutritional supplementation with high
caloric and protein diets, antioxidents,
haematinics and omega 3 fatty acids, arginine .
 Maternal oxygen therapy: Adminitration of 55%
oxygen at a rate of 8L/min round the clock has
shown decreased perinatal mortality rate.
Pharmacological therapy
Aspirin in low doses(1-2 mg/kg body wt.) have
been tried but all have failed to show any
significant difference in incidence of IUGR.
Thus there is no form of therapy currently
available which can reverse IUGR, the only
intervention possible in most cases is delivery.
Delivery
• Since IUGR fetus is at increased risk of
intrauterine hypoxia and intrauterine demise,
the decision needs to delicately balance the
risk to the fetus in utero with continuation of
pregnancy and that of prematurity if delivered
before term.
The optimum timing of delivery is
determined by
• Gestational age,
• Underlying etiology,
• Possibility of extrauterine survival and
• Fetal condition.
• Strict fetal surveillance is needed to monitor
fetal well being and to detect signs of fetal
compromise
Role of steroids
Antenatal glucocorticoid administration
reduces the incidence of respiratory distress
syndrome, intraventricular hemorrhage and
death in IUGR fetuses weighing less than
1500gm.
Mode of Delivery
Fetuses with significant IUGR should be
preferably delivered in well equiped
centres which can provide intrapartum
continuous fetal heart monitoring , fetal
blood sampling and expert neonatal care.
Vaginal delivery:
can be allowed as long as there is no obstetric
indication for caesarian section and fetal heart
rate is normal.
• Fetuses with major anomaly incompatible
with life should also be delivered vaginally.
Caesarian section
Management of new born
Delivery
Resuscitation
Prevention of heat loss
Hypoglycemia
Hematologic disorders
Congenital infections
Genetic anomalies
Complications of IUGR
Perinatal mortality and morbidity of IUGR infants
is 3-20 times greater than normal infants.
• Antepartum period- increased incidence of-
-still births
-oligohydramnios
IUGR is found in 20% of unexplained stillbirths.
• During labour- higher incidence of-
-meconium aspiration
-fetal distress
-intrapartum fetal death
Complications cont..
• Childhood- increases mortality from-
-infectious diseases
-congenital anomalies
Incidence of cerebral palsy are 4-6 times higher.
Subtle impairment of cognitive performance and
educational underachievement.
• Long term complications- increased risk of
coronary heart disease, hypertension, type II
diabetes mellitus, dyslipidaemia and stroke.
Complications of IUGR contd..
• Neonatal period-
• increased incidence of-
-Hypoxic ischemic encephalopathy
-Persistent fetal circulation insufficiency
They have difficulty in temperature regulation
because of absent brown fat and small body
mass relative to surface area.
Lack of glycogen stores may predispose to
hypoglycemia
Chronic intrauterine hypoxia may lead to
polycythemia, necrotizing enterocolitis, other
metabolic abnormalities.
Prognosis
• Mortality increases with prematurity.
• Neurodevelopmental morbidities are seen 5-
10 times more often in IUGR infants.
IUGR

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IUGR

  • 1. Intrauterine Growth RestrictionIntrauterine Growth Restriction (IUGR)(IUGR) Dr. Amlendra Kumar YadavDr. Amlendra Kumar Yadav
  • 2. Definition Failure of the fetus to reach growth potential associated with increased morbidity and mortality Ponderal index less than 10th centile. (used to identify infants whose soft tissue mass is bellow normal for the stsge of skeletal development) Birthweight x 100 Ponderal index = Crown –heel length³
  • 3.
  • 4. IUGR Facts • IUGR associated with 3-10 % of all pregnancies • Perinatal mortality rate is 5-20 times higher for growth retarded fetuses . • 2nd leading contributor to the Perinatal mortality rate • 20% of all stillbirths are IUGR • Incidence of intrapartum asphyxia in cases of IUGR has been reported to be 50%. • Early and proper identification and management lowers this perinatal mortality and morbidity
  • 5. Incidence of IUGR in Bangladesh According to National Low Birth Weight Survey of Bangladesh Low birth weight (<2500g) affects 36% of infants in Bangladesh At least 77% of LBW infants were growth retarded
  • 6. Normal Fetal Growth • Normal fetal growth is characterized by cellular hyperplasia followed by hyperplasia and hypertrophy and lastly by hypertrophy alone.
  • 7. Normal Intrauterine Growth Stage 1 Stage 2 Stage 3 Hyperplasia Hyperplasia/ hypertrophy Hypertrophy 4-20 weeks 20-28 weeks 28-40 weeks Rapid mitosis Declining mitosis Rapid hypertrophy Increasing DNA content Increasing cell size Rapid increasing cell size rapid accumulation of fat, muscle, connective tissue Symmetric Mixed- asymmetric Asymmetric
  • 8. Weight gain • Fetal growth accelerates from about 5g per day at 14 -15 wks of gestation to • 10g per day at 20 wks • Peaks at 30 -35g per day at 32-34wks • After which growth rate decreases. Fetal Growth Indices
  • 9. • Symphysiofundal height increases by about 1cm per wk between 14 and 32 wks. • Abdominal girth increases by 1 inch per wk after 30 wks. It is about 30 inches at 30wks in an average built woman.
  • 10. Classification of Inrauterine Growth Restriction 1. Symmetrical IUGR 2. Asymmetrical IUGR
  • 11. Symmetrical IUGR Head circumference, length, and weight are all proportionally reduced for grstational age (below 10th percentile). It is due to either decreased growth potential of the fetus or extrinsic conditions that are active in pregnancy . Asymmetrical IUGR Fetal weight is reduced out of proportion to length and head circumference . The usual causes are uteroplacental insufficiency, maternal malnutrition, or extrinsic conditions appearing late in pregnancy.
  • 12. Aetiology • IUGR is a manifestation of fetal, maternal and placental disorders that affect fetal growth. A.Fetal Causes 1. Chromosomal Disorders- usually result in early onset IUGR.  Trisomies 13, 18, 21 contribute to 5% of IUGR cases  Sex chromosome disorders are frequently lethal, fetuses that survive may have growth restriction (Turner Syndrome)
  • 13. Fetal causes contd.. 2. Congenital Infections: • The growth potential of fetus may be severely impaired by intrauterine infections. • The timing of infection is crucial as the resultant effects depends on the phase of organogenesis. • Viruses- rubella, CMV, varicella and HIV  rubella is the most embryotoxic virus, it cause capillary endothelial damage during organogenesis and impairs fetal growth.  CMV causes cytolysis and localized necrosis in fetus. • Protozoa- like malaria, toxoplasma, trypanosoma have also been associated with growth restriction.
  • 14. Fetal causes contd.. 3. Structural Anomalies- All major structural defects involving CNS,CVS,GIT, Genitourinary and musculoskeletal system are associated with increased risk of fetal growth restriction. If growth restriction is associated with polyhydramnios, the incidence of structural anomaly is substantially increased.
  • 15. Fetal causes contd.. 4. Genetic Causes- Maternal genes have greater influence on fetal growth. Inborn errors of metabolism like agenesis of pancreas, congenital lipodystrophy, galactosemia, phenylketonuria also result in growth restriction of fetus.
  • 16. B. Placental causes • Placenta is the sole channel for nutrition and oxygen supply to the fetus. Single umblical artery abnormal placental implantation velamentous umblical cord insertion bilobed placenta placental haemangiomas have all been associated with fetal growth restriction
  • 17. C. Maternal Causes 1. Maternal Characteristics: those contributing to IUGR are-  Extremes of maternal age  Grandmultiparity  History of IUGR in previous pregnancy  Low maternal weight gain in pregnancy
  • 18. 2. Maternal diseases: Uteroplacental insufficiency resulting from medical complications like  Hypertension  Renal disease  Autoimmune disease  Hyperthyroidism  Long term insulin dependent diabetes
  • 19. Maternal causes contd.. • Smoking- active or passive, especially during third trimester is important cause of IUGR. Nicotine has vasoconstrctive effect on the maternal circulation and leads to formaton of toxic metabolites in fetus. • Alchohol and Drugs- Alchohol crosses the placenta freely. It acts as a cellular poison reducing fetal growth potential. • Cocaine and opiates are potent vasoconstrictors. • Warfarin, anticonvulsants and antineoplastic agents are also implicated in growth restriction
  • 20. • Thrombophilias- antiphospholipid antibody syndrome and other thrombophilias leading to placental thrombosis and impaired trophoblastic function. • Nutritional Deficiency- leads to deficient substrate supply to the fetus
  • 21. Diagnosis of IUGR Identifying mothers at risk: Poor maternal nutrition Poor BMI at conception Pre-eclampsia Renal disorders Diseases causes vascular insufficiency Infections (TORCH) Poor maternal wt. gain during pregnancy
  • 22. • Determination of gestational age is of utmost importance- – Can be calculated from the date of LMP- not reliable – Ultrasound dating before 21 wks of pregnancy provides more accurate estimate.
  • 23. Diagnosis of IUGR 1. Clinically- Serial measurement of fundal height and abdominal girth.  Symphysio-fundal height normally increases by 1cm per wk b/w 14 and 32 wks.  A lag in fundal ht. of 4wks is suggestive of moderate IUGR.  A lag of >6 wks is suggestive of severe IUGR.
  • 24. Sonographic evaluation- Fetal biometry: i. BPD(Biparietal Diameter)- When growth rate of BPD is below 5th percentile, 82% of births are below 10th percentile
  • 25. ii. Abdominal circumference AC and fetal wt are most accurate ultrasound parameters for diagnosis of IUGR. AC < 5mm/wk reduction is suggestive of IUGR iii. Measurement ratios- there are some age independent ratios to detect IUGR HC/AC: Persistence of a head to abdomen ratio <1 late in gestation is predictive of asymmetric IUGR. Femur length : serial measurements of femur length are effective for detecting symmetric IUGR
  • 26.  Placental Morphology: Acceleration of placental maturation may occur with IUGR .  Placental volume: helpful in predicting subsequent fetal growth.  Amniotic fluid volume: Amniotic fluid index(AFI) between 8 and 25 is normal.
  • 27. Doppler Ultrasonography Doppler flow studies are important adjuncts to fetal biometry in identifying the IUGR fetuses at risk of adverse outcome. Uterine artery flow abnormalities: predict IUGR as early as 12-14 wks of gestation Umblical Artery doppler:- In IUGR there is increased umblical artery resistance
  • 28. Middle cerebral artery doppler: in a normal fetus has relatively little flow during diastole. Increased resistance to blood flow in placenta results in redistribution of cardiac output to favour cardiac and cerebral circulations leading to increased flow in the diastolic phase
  • 29. Ductus venosus doppler In the normal fetus, flow in the ductus venosus is forwards , moving towards the heart during entire cardiac cycle. When circulatory compensation of the fetus fails, the ductus venosus waveform shows absent or reverse blood flow during atrial contraction. Perinatal mortality being 63-100%.
  • 30. Sequential changes of doppler studies in decompensating fetal growth restriction Initial changes Decreased amniotic fluid index Increased uterine artery resistance with EDV Early changes (in 50% 2-3 wks before nonreactive FHR) Decreased MCA resistance (brain sparing ) Absent uterine artery EDV Late changes ~ 6 days before nonreactive FHR Increased resistance in DV-reversed EDV in uterine artery Very late changes (in 70%, 24 hrs before changes in BPP) Reversed flow in DV and pulsatile flow in umbilical vein ( BPP- biophysical profile , DV- ductus venosus, EDV – end diastolic velocity, FHR- fetal heart rate , MCA – mmiddle cerebral artery )
  • 31. Placental magnetic resonance imaging : • Asses severity of fetal growth retardation on the basis of decreased placental volume and thickness.
  • 32. Neonatal Assessment • Reduced birth weight for gestational age • Physical appearance: thin loose, peeling skin, scaphoid abdomen, dispropotionately large head • Appropriate growth charts should be used • Ponderal index • Ballard score
  • 33. MANAGEMENT  Principles: 1. Identify the cause of growth restriction. 2. Treat the cause if found. 3. General management
  • 34. MANAGEMENT  First step is to identify the aetiology of IUGR:- Maternal history pertaining to the risk factors of IUGR. Clinical examination- maternal habitus, height, weight, BP etc.
  • 35. Laboratory investigations Hb, HCT to detect polycythemia Blood sugar Renal function tests, Serology for TORCH
  • 36. Fetal evaluation • Ultrasound for growth restriction, amniotic fluid, congenital anomalies and • Doppler evaluation
  • 37. Treatment of underlying cause  Hypertension,  Cessation of smoking,  Protein energy supplementation in poorly nourished and underweight women.
  • 38. General Management  Bed rest in left lateral position to increase uteroplacental blood flow  Maternal nutritional supplementation with high caloric and protein diets, antioxidents, haematinics and omega 3 fatty acids, arginine .  Maternal oxygen therapy: Adminitration of 55% oxygen at a rate of 8L/min round the clock has shown decreased perinatal mortality rate.
  • 39. Pharmacological therapy Aspirin in low doses(1-2 mg/kg body wt.) have been tried but all have failed to show any significant difference in incidence of IUGR. Thus there is no form of therapy currently available which can reverse IUGR, the only intervention possible in most cases is delivery.
  • 40. Delivery • Since IUGR fetus is at increased risk of intrauterine hypoxia and intrauterine demise, the decision needs to delicately balance the risk to the fetus in utero with continuation of pregnancy and that of prematurity if delivered before term.
  • 41. The optimum timing of delivery is determined by • Gestational age, • Underlying etiology, • Possibility of extrauterine survival and • Fetal condition. • Strict fetal surveillance is needed to monitor fetal well being and to detect signs of fetal compromise
  • 42. Role of steroids Antenatal glucocorticoid administration reduces the incidence of respiratory distress syndrome, intraventricular hemorrhage and death in IUGR fetuses weighing less than 1500gm.
  • 43. Mode of Delivery Fetuses with significant IUGR should be preferably delivered in well equiped centres which can provide intrapartum continuous fetal heart monitoring , fetal blood sampling and expert neonatal care.
  • 44. Vaginal delivery: can be allowed as long as there is no obstetric indication for caesarian section and fetal heart rate is normal. • Fetuses with major anomaly incompatible with life should also be delivered vaginally. Caesarian section
  • 45. Management of new born Delivery Resuscitation Prevention of heat loss Hypoglycemia Hematologic disorders Congenital infections Genetic anomalies
  • 46. Complications of IUGR Perinatal mortality and morbidity of IUGR infants is 3-20 times greater than normal infants. • Antepartum period- increased incidence of- -still births -oligohydramnios IUGR is found in 20% of unexplained stillbirths. • During labour- higher incidence of- -meconium aspiration -fetal distress -intrapartum fetal death
  • 47. Complications cont.. • Childhood- increases mortality from- -infectious diseases -congenital anomalies Incidence of cerebral palsy are 4-6 times higher. Subtle impairment of cognitive performance and educational underachievement. • Long term complications- increased risk of coronary heart disease, hypertension, type II diabetes mellitus, dyslipidaemia and stroke.
  • 48. Complications of IUGR contd.. • Neonatal period- • increased incidence of- -Hypoxic ischemic encephalopathy -Persistent fetal circulation insufficiency
  • 49. They have difficulty in temperature regulation because of absent brown fat and small body mass relative to surface area. Lack of glycogen stores may predispose to hypoglycemia Chronic intrauterine hypoxia may lead to polycythemia, necrotizing enterocolitis, other metabolic abnormalities.
  • 50. Prognosis • Mortality increases with prematurity. • Neurodevelopmental morbidities are seen 5- 10 times more often in IUGR infants.